A second 90 day incubation experiment investigated changes to soil available P and sorption-desorption across variable rates of amendments (0-50&nbsp;g&nbsp;kg-1). Results showed that alum amendment at a rate of 50&nbsp;g&nbsp;kg-1 decreased soil CaCl2-P and Olsen-P concentrations by 91.9% and 57.8%, respectively. However, Olsen-P increased when the dolomite rates were 10&nbsp;g&nbsp;kg-1) could sorb more P in comparison with alum when P concentrations were increased. The P status of the amended soil was closely connected to the P sorption mechanisms on mineral amendments, soil P concentrations and soil properties. Di-(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer, which can enter the body through a variety of ways and exerted multiple harmful effects, including liver toxicity, reproductive toxicity and even glucose metabolism disorder. Many studies have suggested that changes of gut microbiota are closely related to the occurrence of various diseases, but the effects of DEHP exposure on gut microbiota are still unclear. It was found in this study that the damage to different tissues by DEHP on two strains each from two different species of male rodents before puberty was dose and time of exposure dependent, and also depending on the strain and species of rodent. Sprague-Dawley (SD) rats showed highest sensitivity to DEHP exposure, with most severe organ damage, highest Th1 inflammatory response and most significant body weight gain. Correspondingly, the gut microbiota of SD rats showed most significant changes after DEHP exposure. Only SD rats, but not Wistar rats, BALB/c and C57BL/6J mice showed an increase in Firmicutes/Bacteroidetes ratio and Proteobacteria abundance in the fecal samples, which are known to associate with obesity and diabetes. https://www.selleckchem.com/products/drb18.html This is consistent with the increasing body weight gain which was only found in SD rats. In addition, the decrease in the level of butyrate, increase in the abundance of potential pathogens and microbial genes linked to colorectal cancer, Parkinson's disease, and type 2 diabetes in the SD rats were associated with issue and functional damages and Th1 inflammatory response caused by DEHP exposure. We postulate that the differential effects of DEHP on gut microbiota may be an important cause of the differences in the toxicity on different strains and species of rodents to DEHP. Humans are potentially exposed to nano(micro)plastics, however their interaction with tissues and cells in humans remains largely unknown. This premise is particularly notable with nano-sized plastic particulates, a potentially most pernicious form of plastic pollution. In this study, even in a hypothetical scenario in terms of dose (1, 3, 6 and 10&nbsp;mg/kg-day) and exposure time (five weeks), the potential endocrine disturbances with particular reference to reproductive toxicity of polystyrene nanoplastics (PS NPs, average size&nbsp;=&nbsp;38.92&nbsp;nm) was studied in male rats considering biomarkers of semen quality, changes in hormonal milieu and molecular signatures of endocrine disruption. Sperm DNA integrity and its chromatin structure were also analyzed. There observed significant inverse associations between exposure to PS NPs and serum concentrations of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Tissue and cell impairments were also noticed even at the lowest tested dosage, though roblem is growing and will persist for a long time. Air pollutants have been reported to be a possible risk factor of chronic kidney disease (CKD). However, epidemiologic results regarding acidic gases and CKD have yet to be elucidated. We linked the Taiwan Air Quality Monitoring Database (TAQMD) to the Longitudinal Health Insurance Database. An observational cohort of 161,970 Taiwan citizens who had not been diagnosed with CKD was formed. The concentrations of air pollutant were classified into four levels based on quartile. Multivariable and univariable Cox proportional hazard regression models were used to assess the risk of developing CKD and end-stage renal disease (ESRD). Compared with Q1-level SO2, exposure to the Q4 level was at a 1.46-fold risk of developing CKD (95% confidence interval [CI]&nbsp;=&nbsp;1.28-1.65) and 1.32-fold risk of ESRD (95% CI&nbsp;=&nbsp;1.03-1.70). Compared with Q1-level NOx, exposure to the Q4 level was at a 1.39-fold higher risk of developing CKD (95% CI&nbsp;=&nbsp;1.22-1.58) and 1.70-fold risk of ESRD (95% CI&nbsp;=&nbsp;1.33-2.18). Compared with Q1-level NO, exposure to the Q4 level was at a 1.48-fold risk of CKD (95% CI&nbsp;=&nbsp;1.30-1.68) and 1.54-fold risk of ESRD (95% CI&nbsp;=&nbsp;1.20-1.98). Compared with Q1-level particles less then 2.5 μm (PM2.5), exposure to the Q4 level were at a 1.74-fold risk of CKD (95% CI&nbsp;=&nbsp;1.53-1.98) and 1.69-fold risk of ESRD (95% CI&nbsp;=&nbsp;1.32-2.16). Exposure to particulate and acidic gas air pollution was observed to be associated with an increased risk of CKD and ESRD. F-53B and PFOS are two per- and polyfluoroalkyl substances (PFASs) widely utilized in the metal plating industry as mist suppressants. Recent epidemiological studies have linked PFASs to cardiovascular diseases and alterations in heart geometry. However, we still have limited understanding of the effects of F-53B and PFOS on the developing heart. In this study, we employed a human embryonic stem cell (hESC)-based cardiac differentiation system and whole transcriptomics analyses to evaluate the potential developmental cardiac toxicity of F-53B and PFOS. We utilized F-53B and PFOS concentrations of 0.1-60&nbsp;μM, covering the levels detected in human blood samples. We demonstrated that both F-53B and PFOS inhibited cardiac differentiation and promoted epicardial specification via upregulation of the WNT signaling pathway. Most importantly, the effects of F-53B were more robust than those of PFOS. This was because F-53B treatment disrupted the expression of more genes and led to lower cardiac differentiation efficiency. These findings imply that F-53B may not be a safe replacement for PFOS. Hydroquinone (HQ), one of the main metabolites of benzene, is a well-known human leukemogen. However, the specific mechanism of how benzene or HQ contributes to the development of leukemia is unknown. In a previous study, we demonstrated the upregulation of DNA methyltransferase (DNMT) expression in HQ-induced malignant transformed TK6 (HQ-TK6) cells. Here, we investigated whether a regulatory loop between the long noncoding RNA FAS-AS1 and DNMT3b exists in HQ-TK6 cells and benzene-exposed workers. We found that the expression of FAS-AS1 was downregulated in HQ-TK6 cells and workers exposed to benzene longer than 1.5 years via histone acetylation, and FAS-AS1 expression was negatively correlated with the time of benzene exposure. Restoration of FAS-AS1 in HQ-TK6 cells promoted apoptosis and inhibited tumorigenicity in female nude mice. Interestingly, treatment with a DNMT inhibitor (5-aza-2-deoxycytidine), histone deacetylase inhibitor (trichostatin A), or DNMT3b knockout led to increased FAS-AS1 through increased H3K27ac protein expression in HQ-TK6 cells, and DNMT3b knockout decreased H3K27ac and DNMT3b enrichment to the FAS-AS1 promoter region, which suggested that DNMT3b and/or histone acetylation involve FAS-AS1 expression.